Vol. 22, No.
12 December 2000
CE Refereed Peer Review
FOCAL POINT
★The pathogenesis of canine
gastric dilatation-volvulus (GDV)
remains a complex multifactorial
event that probably differs
from patient to patient, but
two discrete pathogenetic
mechanisms are likely to
give rise to this syndrome.
KEY FACTS
■ The pathogenesis of GDV
remains complex and poorly
understood.
■ Although the precise mechanism
of gastric volvulus remains
unclear, several intrinsic and
extrinsic risk factors have been
identified.
■ Failure of the normal eructation
and pyloric outflow mechanisms
is a fundamental prerequisite for
the development of gastric
dilation.
■ Whether gastric volvulus
consistently precedes or follows
gastric dilation is unclear, but
both scenarios seem plausible
and likely.
Pathogenesis of Acute
Canine Gastric
Dilatation–Volvulus
Syndrome: Is There a
Unifying Hypothesis?*
University of Pennsylvania
Daniel J. Brockman, BVSc
David E. Holt, BVSc.
Robert J Washabau, VMD, PhD
ABSTRACT: A single etiologic agent in the pathogenesis of acute canine gastric dilatation-
volvulus (GDV) has not yet been identified. Several extrinsic physical and environmental risk
factors have been identified, and many more intrinsic anatomic or pathologic risk factors are
suspected. Many of the proposed intrinsic factors currently lack scientific evidence, and it may
be impossible to substantiate these factors. Normal eructation, vomiting, or pyloric outflow
mechanisms appear to fail when gastric dilation occurs. Whether volvulus consistently pre-
cedes or follows dilation is unclear. This paper explores the known risk factors for GDV and
proposes a hypothesis to explain its pathogenesis.
M
uch has been learned about the pathophysiology and clinical manage-
ment of canine acute gastric dilatation–volvulus (GDV), but a unify-
ing hypothesis for the pathogenesis of this syndrome has not yet been
elucidated. Several theories have been proposed, but most do not readily explain
all clinical findings.
A unifying hypothesis must be capable of answering or addressing several im-
portant questions: Why are large- and giant-breed dogs at greater risk than are
small breeds? If body size and thoracoabdominal dimensions are important fac-
tors, why is GDV not more common in relevant breeds? If volvulus is believed
to be the initiating event, why are some animals observed with dilation alone? If
volvulus induces obstruction and dilation, why do some animals occasionally
*A companion article entitled “Management Protocol for Acute Gastric Dilatation–
Volvulus Syndrome in Dogs” appeared in the November 2000 (Vol. 22 No. 11) issue of
Compendium.
Compendium December 2000
present with chronic volvulus but without dilation?
Why are certain breeds more affected than are others?
Are there genetic influences, or do differences in feed-
ing practices or other environmental factors play a role
in this syndrome? This paper reviews the relevant in-
trinsic and extrinsic factors that have been proposed to
determine whether a single unifying hypothesis can ex-
plain the pathogenesis of GDV.
INTRINSIC FACTORS
Body Size
Acute canine GDV is predominantly a disease of
large body conformation.1 Small dogs appear only spo-
radically in the large case studies and single case reports
describing this condition2–4; therefore, anatomic and
genetic features are assumed to predispose large- and gi-
ant-breed dogs to this condition.
Thoracoabdominal Dimensions
Risk factor analysis supports the notion that thoracic
conformation is an important factor in the develop-
ment of GDV. Studies have shown that increased tho-
racic depth:width ratios are associated with increased
risk of development of this syndrome within certain
breeds.5,6 Those studies caused further speculation that
selective breeding against deep-chest conformation
would decrease the prevalence of GDV within breeds.5,6
Despite the apparent association, it is unclear how tho-
racic and abdominal dimensions influence the develop-
ment of GDV. Accentuated thoracic and abdominal di-
mensions have been suggested to play a permissive or
active role in the initiation of GDV by virtue of altered
position of the gastric cardia.7 Although a relationship
between thoracoabdominal conformation and GDV
has been identified, the mechanism of its influence is
unclear.
Gastric Ligament Laxity
The canine stomach has evolved to accommodate
varying meal size and frequency and, therefore, varying
degrees of distention. Gastric ligaments (i.e., lesser
omental, greater omental, mesoduodenal) hold the
stomach loosely in position to accommodate changes in
gastric volume and muscular activity. Despite this
anatomic configuration, gastric ligaments do not pre-
vent clockwise rotation of the stomach in canine cadav-
ers or in experimental animals.8,9 Thus laxity of gastric
ligaments appears to be sufficient to permit gastric rota-
tion even in healthy dogs.
In addition, dogs with GDV may have reduced abili-
ty to resolve gastric rotation10 based on the observation
that the stomachs of dogs that have had GDV maintain
the same clockwise-rotated position. In contrast, the
DEEP-CHEST CONFORMATION ■ GASTRIC ROTATION ■ HYPERGASTRINEMIA
Small Animal/Exotics
stomachs of dogs that have not had GDV return to a
normal position after such a rotation.10 More recently,
the hepatogastric ligaments of dogs with GDV were
shown to be longer than were non-GDV size- and
weight-matched controls.11 Abnormalities (e.g., length,
elasticity) may contribute to episodes of GDV, but this
has not yet been shown in the pre-GDV state.
Gastric Volume
Once-daily feedings were found to be a predisposing
risk factor for the development of gastric dilation (GD)
in Irish setters.12 Once-daily feedings may induce in-
creases in intragastric volume in this breed when com-
pared with three-times-daily feeding.13 Whether or how
gastric volume influences the occurrence of GDV is un-
known. A consistent feeding pattern is not apparent
among the majority of GDV patients reported in the
literature. Once-daily feeding may increase risk of GD
and GDV in Irish setters, but it is unclear whether
once-daily feedings pose a risk for other breeds.
Hormonal Influences
Mild hypergastrinemia was documented in a group
of dogs with acute GDV that were in a fasting state fol-
lowing recovery from surgery.14 Results from this study
suggest that preexisting hypergastrinemia may con-
tribute to an increased incidence of GDV because of
pharmacologic effects of gastrin on increasing lower
gastroesophageal sphincter (GES) tone, promoting gas-
tric mucosal hyperplasia and muscular hypertrophy,
and inhibiting gastric emptying. Subsequent studies15
have failed to reveal consistent hypergastrinemia in
post-GDV dogs. Further, gastric distention in clinically
normal dogs does not induce significant increases in
plasma gastrin immunoreactivity or lower GES pres-
sure. Thus there is insufficient evidence to support a
role for the gastrointestinal (GI) hormone gastrin in the
pathogenesis of canine GDV complex. The roles of
other GI hormones, particularly those involved in the
regulation of GI motility (e.g., motilin, cholecystoki-
nin), have not yet been investigated.
Gastric Position
Thoracoabdominal dimensions may influence the
resting position of the stomach and, therefore, the
gastric cardia and abdominal esophagus.7 It has been
suggested that altered conformation may interfere
with the normal mechanism of eructation and vomit-
ing.7 Although conjectural, this theory may explain
why some animals have chronic GD after acute GDV
therapy. The effects of gastric position on gastric dis-
tention and GDV development is complex. Based on
their study of canine cadavers, Blackburn and Mac-
Small Animal/Exotics
Farlane8 concluded that GD only resulted in GDV if
the stomach was already malpositioned. This obser-
vation has led many investigators to consider other
factors such as the influence of the spleen, exercise,
and concurrent inflammatory GI disease as well as
meal size and frequency. The fact that GDV can oc-
cur in splenectomized dogs16 suggests that it is not es-
sential in the pathogenesis of GDV in all dogs.
Similarly, meal type and feeding frequency are not
consistent among GDV patients, ruling out diet as a
common etiologic factor. Some dogs clearly tolerate
gastric volvulus (without dilation) for extended peri-
ods.17,18 Consequently, if the stomach is rotated, its
malposition could influence both eructation and py-
loric function and thereby lead to dilation. Incom-
plete GES and pyloric dysfunction in some volvulus
patients may permit gas to escape through eructation,
gastric emptying, or absorption.
Eructation
The initiation of eructation and the vomiting reflex
occurs at intragastric pressures lower than those record-
ed from spontaneous cases of GDV.19–21 Factors that can
independently influence the eructation mechanism in-
clude sleep, certain anesthetic drugs, and damage or in-
filtration of the vagus nerve or gastric cardia.19,20,22,23
Transient relaxation of the GES following gastric fun-
dus distention is an important mechanism for eructa-
tion in dogs.23 Presumably, gastric volvulus mechanical-
ly interferes with eructation. If gastric volvulus always
preceded GDV, disordered eructation could be easily
explained. In situations in which GD precedes GDV,
the question of what prevents gastric decompression—
either eructation of gas or vomiting of solids—remains.
When dogs were gorge-fed in an attempt to create
GDV, gastric decompression was achieved rapidly by
opening the pyloric canal, vomiting, or both.24 Even if
the eructation mechanisms were defective, given that
gastric decompression can also be achieved by opening
the pyloric canal, failure to eructate or vomit alone
should not necessarily initiate GD. Acute failure of the
eructation and vomiting mechanism must occur in
GDV-affected dogs, perhaps with simultaneous pyloric
dysfunction; therefore, disorders of eructation and
vomiting most likely contribute to the initiation of
GDV.
Gastric Rhythm, Motility, and Emptying
Funkquist and Garmer25 demonstrated that the gas-
tric emptying of a liquid barium meal was delayed in
animals recovering from GDV. This study was prompt-
ed by the observation that several of the animals that
presented with GDV had historical evidence of chronic
PYLORIC CANAL ■ GASTRIC EMPTYING ■ CHRONIC VOMITING
Compendium December 2000
vomiting.25 Together with the fact that some dogs had
recurrent episodes of GD following otherwise success-
ful therapy for GDV,26 this evidence suggested the pres-
ence of a primary gastric emptying disorder. In addi-
tion, spontaneous gastric decompression normally occurs
at intragastric pressures far lower than those reported
for naturally occurring GDV.19,20,27 Gastric dysrhyth-
mias, eructation disorders, and abnormal pyloric func-
tion were suspected to be initiating factors. These fac-
tors could influence gastric contents, degree of fill, and
gastric position, thereby leading to GDV.
Funkquist and Garmer25 demonstrated delayed gas-
tric emptying of a liquid barium sulfate suspension in
dogs recovering from GDV, suggesting that delayed
gastric emptying played a role in the pathogenesis of
this syndrome. A subsequent study that measured gas-
tric emptying (using a radiolabeled test meal adminis-
tered after recovery from GDV and tube gastropexy)
failed to show a difference compared with nondiseased
controls.28 Yet another study29 using radiopaque mark-
ers determined abnormalities of gastric emptying
among dogs that had recovered from GDV and cir-
cumcostal gastropexy. These experiments used different
methods to evaluate gastric emptying; the timing of the
evaluation relative to the acute episode of GDV varied.
Typically, dogs with longstanding delayed gastric
emptying are presented because of chronic vomiting, as
was seen by Funkquist and Garmer.25 Data from own-
ers of dogs with GDV, however, have rarely indicated a
clinical syndrome associated with chronic delayed gas-
tric emptying before the acute GDV episode. In addi-
tion, results of a clinical trial by Greenfield and col-
leagues30 suggested that pyloric modification, in an
attempt to enhance pyloric outflow, caused increased
morbidity without demonstrable enhancement of gas-
tric emptying and could not be justified. These obser-
vations suggest that the delayed gastric emptying that is
seen experimentally may be the result—rather than the
initiator—of GDV and its treatment. Evidence for
chronic gastric outflow obstruction in all GDV patients
is lacking, and pyloric modification cannot be recom-
mended as routine.
Acute pyloric dysfunction, however, is influential in
GDV. The pyloric canal normally opens to allow aboral
passage of gastric contents at intragastric pressures of 8
to 14 mm Hg,27 far lower than intragastric pressure
recorded from clinical cases of GDV.21 Stress, elec-
trolyte disturbances, and certain anesthetic agents can
influence pyloric function and delay gastric emptying.
In a recent study,12 stress associated with car rides or
placement in boarding kennels was calculated as a risk
factor for GDV. Obversely, gastric malposition could
mechanically interfere with pyloric outflow. Therefore,
Compendium December 2000
it is likely that acute pyloric dysfunction exists. Logical-
ly, pyloric dysfunction could be either the cause of
GDV or the result of gastric malposition. Therefore, its
role in this disease may vary from dog to dog. Disor-
ders of gastric myoelectrical and mechanical activity
can influence gastric emptying and could conceivably
initiate an episode of GDV. Evidence for such myoelec-
trical disorders in dogs recovering from GDV exists.31,32
Unfortunately, further investigation of the relationship
between gastric dysrhythmias and the onset of GDV
has been hampered by the lack of practical noninvasive
techniques to make such measurements, and the lack of
resources needed to screen the large at-risk population.
Age
Although GDV may occur at any age, there is a
greater risk of occurrence in older dogs.1 Increasing age,
however, has not been linked with higher mortality.2,3
Sleep
In humans, transient lower GES relaxations induced
by gastric fundic distention are apparently abolished
during stable sleep.33 Although not yet studied in dogs,
this scenario is most likely true in sleeping dogs as well
because fundic distention–induced GES relaxations are
under the same physiologic regulation as in humans.
Fundic distention–induced transient GES relaxations
are important in mediating eructation in both dogs and
humans. 19,20,23 This theory may explain why some
episodes of GDV have been anecdotally associated with
sleep34 and anesthetic events.
EXTRINSIC FACTORS
A synthesis of the events leading up to an episode of
GDV and the observations by clinicians caring for ani-
mals with this disease have led to a myriad of putative
initiators of GDV.28 The identification of risk factors
should enable veterinarians to advise clients on how to
avoid these risks.
Diet
The increased incidence of GDV coincided with the
use of plant protein (especially soybean meal) by the
pet food industry.24 Some reports have also associated a
sudden change in diet with precipitation of GDV.35
Others have reported a decrease in the prevalence of
GDV associated with altered feeding habits among hos-
pitalized animals.7 More recently, once-daily feeding
and feeding a single food type were calculated to be risk
factors for GD among Irish setters in the United King-
dom.12 Interest, therefore, has focused on the influence
of diet composition and feeding frequency on the de-
velopment of GDV.13,31
PLANT PROTEIN ■ FEEDING PATTERNS ■ INTRAGASTRIC FERMENTATION
Small Animal/Exotics
Postprandial Gastric Dilation
Abnormally large meals and/or the consumption of a
large amount of water have been associated with the on-
set of clinical signs of GDV.3,12 Some researchers have
hypothesized that dogs with acute GD that consume a
large quantity of food and fluids could mediate GDV by
altering the position of the gastric cardia, thereby inter-
fering with eructation and vomiting.7 Others have spec-
ulated that the weight of a large meal in the stomach,
especially when coupled with physical exertion, could
mediate gastric rotation by acting like a pendulum.8
Again, the feeding patterns reported for dogs with GDV
are varied, and GD initiated predominantly by food or
liquid consumption is rare. Food type and composition
were not found to have an effect on gastric emptying
time and postprandial gastric motility patterns when fed
isocalorically to dogs.31 Attempts to induce GDV by en-
gorging dogs with food failed in one study.24 Alterations
in feeding and exercise patterns also failed to alter the
incidence of GDV in a large population of military dogs
reported by the same researchers.24 The relationship be-
tween meal volume, postprandial GD, and GDV re-
mains unclear. Diet composition and feeding frequency
seem to be insignificant factors for most dogs.
Accumulation of Gastric Gas
In most dogs with GDV, the stomach is distended pre-
dominantly by gas. The origin of this gas has been the
subject of several studies.36,37 The suggestion that certain
diets contained fermentable substrates36 and favored the
formation of intragastric gas gained temporary accep-
tance. These feeds, therefore, predisposed dogs to GDV
by virtue of gas production that exceeded normal mecha-
nisms for gastric gas dispersal. Evidence for intragastric
fermentation of food was found by analyzing gas from
the stomachs of dogs that died of GDV. The gas compo-
sition included the presence of volatile fatty acids, further
suggesting intragastric fermentation.36 Normally, the acid-
ity within the gastric lumen precludes the presence of
most bacteria, with Clostridium perfringens being the only
organism consistently cultured from gastric juice.38 The
possibility exists that the process of GDV causes a rapid
alteration in intragastric pH, permitting bacteria from the
oral cavity to initiate fermentation of food, but scientific
proof of this mechanism is lacking.
In addition, another study that analyzed the gastric gas
of dogs with GDV37 suggested that the source of the gas
was predominantly aerophagia in which additional car-
bon dioxide resulted from the action of gastric acid on
salivary bicarbonate. Aerophagia was recently calculated
to be a risk factor for GDV among Irish setters in the
United Kingdom.12 In addition, van Sluijs26 reported sev-
eral aerophagic dogs that suffered repeated episodes of
Small Animal/Exotics Compendium December 2000

Normal stomach

Anesthesia Trauma Anatomic effects Stress

Nutritional
Anatomic predisposition Vagus nerve Motility effects
(ligaments, thoracic depth:width disruption disorder?
ratio, gastric volume)

Sleep Pyloric obstruction

(neoplasia, foreign body)

Gastroesophageal Pyloric dysfunction

Motility
disorders? sphincter dysfunction and (delayed or impaired
(failure of eructation) gastric emptying)

Transient Anxiety/excitement
gastric
rotation Gastric Aerophagia Dyspnea
fermentation?
Gastric
Rapid eating
volvulus

Anxiety/excitement Motility Gastric

disorder dilation
Aerophagia Dyspnea
Splenic influence
Rapid eating
Postprandial exercise
Gastric
fermentation

Gastric
dilatation–volvulus

Figure 1—Algorithm depicting a unifying hypothesis for the development of gastric dilatation–volvulus syndrome.

GD. Aerophagia, therefore, most likely plays a role in
some dogs, either as an initiating or as an exacerbating
factor for GDV.
PROPOSED HYPOTHESIS FOR THE PATHOGENESIS
OF GASTRIC DILATATION–VOLVULUS
The pathogenesis of GDV is influenced by environ-
mental, anatomic, physiologic, and pathologic risk fac-
tors. The role of each risk factor has been limited by
the inability of researchers to obtain noninvasive data
from the at-risk population. The prevalence of this dis-
ease is estimated to be 0.8%3 to 2.8%7 of veterinary
emergency room and hospital populations, respectively.
With such a low disease prevalence, the statistical pow-

AEROPHAGIA ■ MOTILITY DISORDER ■ AT-RISK POPULATION

 Compendium December 2000
er of measurements and observations made from the at-
risk population will be low. Additional epidemiologic
surveys will be needed to facilitate a better understand-
ing of the pathogenesis of this disease.
We have proposed a unifying hypothesis for the
pathogenesis of GDV syndrome (Figure 1). In this
model, failure of the normal eructation and pyloric
outflow mechanisms is a fundamental prerequisite for
the development of GD. Whether gastric volvulus con-
sistently precedes or follows these events is unclear. We
believe the veterinary literature supports the likelihood
and clinical relevance of both scenarios:
Normal stomach → Gastric volvulus → GES and py-
loric dysfunction → GD/GDV
Normal stomach → GES and pyloric dysfunction →
GD → Volvulus/GDV
We believe this model helps to explain why some ani-
mals are occasionally observed with chronic volvulus but
without dilation (e.g., incomplete GES and pyloric dys-
function in some volvulus patients would permit gas to
escape through eructation, gastric emptying, or absorp-
tion). The model would also explain why many dogs are
observed with acute GD but without volvulus (e.g., gas
DID REACHING A DIAGNOSIS
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PUZZLE US WITH IT, TOO!
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YOUR DIAGNOSIS?” Any intriguing case in veterinary
medicine is welcome. The diagnosis may have turned out
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simply been a stumper. If you have one, send it in.
Articles should be 500 words long, with most of the evidence
presented; the diagnosis itself should be summed up in one to two
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Small Animal/Exotics
may accumulate too quickly to permit rotation of the
stomach). Finally, the model may explain why some
GDV episodes are associated with sleep or anesthesia.
Sleep and anesthesia interfere with the fundic disten-
tion–induced transient relaxations of the GES.
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Small Animal/Exotics
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About the Authors
When this article was submitted for publication, Drs.
Brockman, Holt, and Washabau were affiliated with the
Department of Clinical Sciences and the Center for Veteri-
nary Clinical Care, School of Veterinary Medicine, Univer-
sity of Pennsylvania, Philadelphia. Dr. Brockman is now
affiliated with the Department of Small Animal Medicine
and Surgery, The Royal Veterinary College, University of
London. Drs. Brockman and Holt are Diplomates of the
American College of Veterinary Surgeons. Dr. Washabau
is a Diplomate of the American College of Veterinary Inter-
nal Medicine. Dr. Brockman is also a Diplomate of the Eu-
ropean College of Veterinary Surgeons.